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环磷酸腺苷(cAMP)诱导的NCL-SG3汗腺细胞中的氯离子转运。

cAMP-induced chloride transport in NCL-SG3 sweat gland cells.

作者信息

Mörk A C, von Euler A, Roomans G M, Ring A

机构信息

Department of Human Anatomy, University of Uppsala, Sweden.

出版信息

Acta Physiol Scand. 1996 May;157(1):21-32. doi: 10.1046/j.1365-201X.1996.450223000.x.

Abstract

cAMP-induced ion transport in a human sweat gland cell line, NCL-SG3, was investigated by X-ray microanalysis and patch-clamp technique. Stimulation with cAMP caused a decrease in the cellular Cl and K. cAMP had no significant effect on the intracellular Na and Ca. Chloride channel blockers (9-AC, DPC and NPPB) inhibited the cAMP-induced chloride efflux. In patch-clamp experiments the inward current increased over a period of 5-15 min on addition of membrane-permeable cAMP in 66% of the attempts when the cell was held at 0 mV and pulsed to negative membrane potentials. The inward current was completely blocked by chloride channel blockers. Washout reversed the effect of cAMP. The inward current was not diminished by substitution of impermeable cations for Na in the bath and was insensitive to TEA (tetraethylammoniumchloride). It is concluded that the inward current is mainly a chloride current. Cystic fibrosis transmembrane regulator (CFTR) could not be demonstrated in the NCL-SG3 cells. It is therefore possible that the chloride efflux is mediated by other types of chloride channels.

摘要

采用X射线微量分析和膜片钳技术研究了环磷酸腺苷(cAMP)诱导的人汗腺细胞系NCL-SG3中的离子转运。用cAMP刺激导致细胞内氯离子(Cl)和钾离子(K)减少。cAMP对细胞内钠离子(Na)和钙离子(Ca)无显著影响。氯离子通道阻滞剂(9-AC、DPC和NPPB)抑制了cAMP诱导的氯离子外流。在膜片钳实验中,当细胞保持在0 mV并脉冲至负膜电位时,在66%的实验中,加入膜通透性cAMP后,内向电流在5-15分钟内增加。内向电流被氯离子通道阻滞剂完全阻断。洗脱逆转了cAMP的作用。用不透性阳离子替代浴液中的Na不会减少内向电流,且内向电流对四乙铵(TEA)不敏感。得出的结论是,内向电流主要是氯离子电流。在NCL-SG3细胞中未检测到囊性纤维化跨膜传导调节因子(CFTR)。因此,氯离子外流可能由其他类型的氯离子通道介导。

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